Chronic rejection represents the most important risk factor for poor long-term survival in clinicalheart and lung transplantation [1, 2]. In most cases, the ultimate cause of graft loss is a slowlydeveloping fibro-occlusive disease, whereby spaces within the organ fill up with collagen-forming cellsand fibrous material which in turn blocks passage of blood and air, ultimately destroying the functionalcapacity of the graft. When identifiable, infiltrates during chronic rejection are relatively enriched formonocytes/macrophages, and tend to lack Thi cytokines [e.g. IL-2 and IFN-y] that predominate in theeariy acute rejection phase [3]. Unfortunately, the immunosuppressive [IS] drugs currently in use fortransplant patients, mainly calcineurin inhibitors [CNI], corticosteroids and purine analogs, can reverseand prevent acute rejection but do little to halt the progress of fibro-obliteration. One possible reason forthe ineffectiveness of CNI drugs in chronic rejection is that CNI drugs target the calcineurin/NFATpathway that induces IFN-y and IL-2, inhibiting function of allospecific Th1 cells and 008